Endoplasmic reticulum stress contributes to arsenic trioxide-induced apoptosis in drug-sensitive and -resistant leukemia cells

被引：33

作者：

Chen, Jing ^{[1
]}

Wei, Hulai ^{[1
]}

Xie, Bei ^{[1
]}

Wang, Bei ^{[1
]}

Cheng, Juan ^{[1
]}

Cheng, Jie ^{[1
]}

机构：

[1] Lanzhou Univ, Key Lab Preclin Study New Drugs Gansu Prov, Sch Basic Med Sci, Lanzhou 730000, Gansu, Peoples R China

来源：

LEUKEMIA RESEARCH | 2012年 / 36卷 / 12期

基金：

中国国家自然科学基金;

关键词：

Arsenic trioxide; Drug resistance; Endoplasmic reticulum stress; Apoptosis; RETINOIC ACID; DEATH PROGRAM; ER STRESS; CANCER; CASPASE; INHIBITION; EXPRESSION; PHARMACOKINETICS; DIFFERENTIATION; PROLIFERATION;

D O I：

10.1016/j.leukres.2012.08.018

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

This study characterized the role of endoplasmic reticulum stress (ERS)-related pathways in arsenic trioxide-induced apoptosis in multidrug-resistant leukemia K562/ADM cells. Arsenic trioxide exposure led to much significant induction of apoptosis in K562/ADM cells than the parental K562 cells, and the chaperone proteins glucose-regulated protein 78, CHOP/GADD153, X-box binding protein-1 and caspase-12 were activated to varying degrees. Furthermore, arsenic trioxide stimulation led to inhibition of Pglycoprotein and Bcl-2 expression. This study demonstrates a missing link between arsenic trioxide and ERS-induced apoptosis, and suggests that the greater effects obtained in drug-resistant K562/ADM cells may be mediated by downregulation of P-glycoprotein and Bcl-2 expression. (C) 2012 Elsevier Ltd. All rights reserved.

引用

页码：1526 / 1535

页数：10

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